February 2019: ALS and nnEMF pollution

Might ALS be a defect in the control stimulus of this process, keeping the injury repair pro-inflammatory for too long?  Might the EMF stimulus in the environment control this energy phase transition?  It is now well known that environmental EMFs can block the phase transition of the inflammatory response to the anti-inflammatory pathways via calcium ion resonance changes. MCP-1 is the critical cytokine in this energy transition in wound healing.  This was the topic of my February webinar of 2019.

IS ALS an electromagnetic abnormality caused by light signal defects in our immune system that destroy motor neurons with little to no melanin?

WHY MELANIN?

Please realize that the number of genes an organism has in its genome is linked to how much energy it can transform. This means the gene expression is also directly correlated by probabilities to how it is expressed. POMC in mammals is critical in this energy linkage. This is a function of the energy/information flow and not the anatomy of the genome itself. It is also related to the redox potential of the organism in question. Ultimately, All energy in life ultimately comes from sunlight. It is stored in every cell membrane and the electronic state of cells. Most of these energy stores available to cells are not accounted for in any biochemistry book. You are dead wrong if you have a biochemical bias for health and think labs can decipher this code. Labs cannot account for any energy stored in the electronic state of cells.  This perspective is the blind spot for functional medicine and centralized medicine.

WHY US URIC ACID A KEY TO UNDERSTANDING ALS

People with uric acid issues are fundamentally solar deficient and cannot heal wounds rapidly.  Moreover, they exhibit poor mitochondrial redox and higher tissue heteroplasmy in the injured areas as a result.

Any time melanin sheets in your CNS/brain are degrading (decreased POMC expression), so is melatonin production from your mitochondria. And remember, melatonin feeds back on all circadian clock genes: a theory involving the proteasome or maybe the exposome?

POMC creates melanin via the multiple cleavage MSH proteins in neuroectodermal derivatives, which directly connect to the mitochondrial layers in the retina via the RPE.  

Moreover, that information is supposed to be shared electromagnetically in cells via the nonvisual photoreceptor system to the brain structures deeper in your skull and spinal cord. How does it all happen, you ask? Read my Twitter lesson below.

https://twitter.com/DrJackKruse/status/1633843206717837312 

The paper below reports, " The interaction of melatonin with the proteasome in the hypothalamus also provides a model for explaining the dramatic 'time-of-day' effect of melatonin injections on the reproductive status of seasonal breeders."

This paper seems to predict that a proteasome inhibitor that acts like sunlight would modify circadian rhythms like melatonin.

The primary function of the proteasome is to degrade proteins.  Melatonin is critical in the ubiquitination process of tissue repair in humans.  Melatonin needs AM solar exposure to induce a DC electric current to induce tissue repair in the motor neurons.  In ALS, degraded misfolded proteins are a key issue in tissue damage of the motor neurons.  Proteasome substrates in mammals include signaling molecules called tumor suppressor genes, cell-cycle regulators (melatonin/UV light), transcription factors (MCP-1), inhibitory molecules (whose degradation activates other proteins) like uric acid, and anti-apoptotic proteins (Bcl-2), among others.  

https://www.ncbi.nlm.nih.gov/pubmed/25369242

SUMMARY

Allopathic and functional medicine is still prehistoric in understanding life and health concerning neurodegenerative conditions. When they want you to order labs, they are putting their hands in your pockets and robbing you blind. They are actually telling you they have no earthly idea what they are doing, but most of you have bought their beliefs of how you monitor health with labs. It is a pure fabrication of a centralized paradigm built on many fallacies.  They do labs because their understanding of the disease is only biochemical and divorced from the biophysics operating in your cells. 

Nitric oxide is stimulated by UV-A light, and when you get enough of this frequency of light, your uric acid levels are controlled easily by the system. If you lack proper solar exposure,   uric acid can become a big issue for wound healing and repair of the non-visual photoreceptors of the anterior motor neurons (below). 

Many epidemiological studies have indicated a strong link between hypouricemia and an increased risk of developing neurological diseases.  

Historically, biochemists have considered uric acid a waste of cellular metabolism, but now it is clear it has a diurnal pattern tied to light cycles.  Uric acid has now received increasing attention because it was found to directly participate in the pathogenesis of many human diseases, including neurological disorders. On the one hand, low levels of UA are detrimental to the neurons because of its induction. It impairs antioxidant capacity in the cell for short durations. On the other hand, high levels of UA lead to a chronic inflammatory response, contributing to neuroprotection. It's now well-established that uric acid has a biphasic function. 

Uric acid has the ability to modify the oxidation state of iron in hemoglobin to slow oxygen and nitric oxide delivery to mitochondria SIMULTANEOUSLY.  This helps increase blood flow while lowering ATP function.  If this system is broken, motor neurons become stressed and die.  It is a biochemical signal that tells us something is awry in the NO system of arteries going to the anterior motor neuron columns that are missing melanin.  

This tells us why ALS is not common in the tropics and is more prominent as we go to the poles.  It also explains why it is linked to electromagnetic toxicity because this alters NO signaling while degrading melanin in the CNS.  

Mitochondrial dysfunction is a hallmark of aging and neurological diseases and is closely interconnected to stem cell exhaustion and cellular senescence.  I think ALS is caused by a rapid upregulation of senescence in motor neurons.  

In general, aging-associated mitochondrial dysfunction is defined as the impairment of mitochondrial morphology and function, characterized by an increase in fragmented mitochondria due to dysregulation of fission, fusion, and mitophagy, as well as accumulated mitochondrial DNA (mtDNA) mutations and increased mitochondrial mass, accompanied by decreased respiratory capacity, damaged mitochondrial membrane potential, and enhanced levels of reactive oxygen species (ROS). Emerging evidence also suggests that mitochondrial activity is mechanistically linked to stem cell exhaustion, including in a type of adult stem cells called mesenchymal stem cells (MSCs), which are resident in multiple tissues and possess capabilities of both self-renewal and linage differentiation in damaged tissues.

Mitochondrial antiviral signaling protein (MAVS), which is essential for driving antiviral response, also regulates human stem cell senescence.  In recent years, data has shown that MAVS plays a KEY role in maintaining mitochondrial structural integrity and functional homeostasis depending on its interaction with the guanosine triphosphatase optic atrophy type 1 (OPA1). Depletion of MAVS or OPA1 leads to the dysfunction of mitochondria and cellular senescence.  This mechanism is key in understanding how motor neurons can be knocked out in isolation.  It tells us the mitochondria of the motor neurons likely have a specific target to explain the disease phenotype.  New evidence now shows that the replenishment of MAVS or OPA1 in MAVS-knockout human mesenchymal cells (hMSCs) alleviated mitochondrial defects and premature senescence phenotypes.  ALS is a neurologic disease that is associated with a premature senescent phenotype of the anterior motor cells.  

Numerous mitochondrial constituents and metabolic products function as damage-associated molecular patterns (DAMPs) and promote inflammation when released into the cytosol or extracellular milieu. Several safeguards (circadian-derived) are normally in place to prevent mitochondria from eliciting detrimental inflammatory reactions, including the autophagic disposal of permeabilized mitochondria. However, when the homeostatic capacity of such systems is exceeded or when such systems are defective, inflammatory reactions elicited by mitochondria can become pathogenic and contribute to the etiology of human disorders linked to the autoreactivity to the mitochondria of specific neurons in the spinal cord and brainstem.  I believe this is what ALS is.  

CITES

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755091/

Paganoni S, Zhang M, Quiroz Zarate A, Jaffa M, Yu H, et al. Uric acid levels predict survival in men with amyotrophic lateral sclerosis. J Neurol. 2012;259:1923–1928.